thiamine, taurine, phosphorus and CFS

[Guest guest]

A call to all researchers out there! Has anyone come across any more

information that suggests taurine helps thiamine metabolism. This was

what Kim Allsup - who I mentioned in a previous post - said in her

original newsgroup postings. I wrote to her a while ago and asked her

which articles she was referring to for her statement (taurine acts

likes a switch for thiamine, etc.).

Note the information about high energy phosphates along with B1, B6

and magnesium in the abstract for the article titled " Effects of

magnesium, high energy phosphates, piracetam and thiamin on

erythrocyte transketolase " .

I've been following the possibility that taurine and phosphorus are

connected in some deeper way and am beginning to think that it might

play some kind of regulatory role in the kidney. I have great article

that I'd like to post to the Files section titled " Taurine, Analogues

and Bone: A Growing Relationship " that suggests that the newest

therapies to prevent bone loss may be taurine derivatives. If anyone

can tell me how to do this, I'd appreciate it.

As a sidenote, there's some interesting research being done on polar

bears that is investigating whether or not taurine deficiency plays a

role in the development of rickets:

http://www.polarbearsalive.org/taurine.php

Adding to that, there's an abstract that suggests a significant number

of people with CFS have phosphate diabetes. Maybe the impaired

thiamin metabolism is coming from phosphate depletion brought on by

abnormalities in taurine production or from deficiency???? I'd love

to hear any one's comments:

Kim Allsup pointed me to the following two articles:

Vopr Med Khim. 1995 Nov-Dec;41(6):36-42.

[On vitamin B1 metabolism in avitaminosis and its correction with

thiamine and taurine]

[Article in Russian]

Chernikevich IP, Gritsenko EA, Lisitskaia IM, Luchko TA.

The levels of phosphate esters and the activities of thiamine

biotransformation enzymes in the blood and tissues of albino rats were

studied during oxythiamine-induced B1 deficiency and after metabolic

correction with thiamine and taurine. Among thiamine phosphates, the

most informative indicators of thiamine deficiency were shown to be

triphosphate esters and free thiamine diphosphate. The biosynthetic

enzymes thiamine kinase and thiamine diphosphate kinase played a

decisive role in maintaining the initial rate and in recovering the

physiologically active forms of vitamin B1. The activation of

hydrolytic enzymes of thiamine phosphate esters occurred by producing

abundant free thiamine diphosphate and thiamine triphosphate. Within

the first hours, taurine favoured the acceleration of phosphoester

biosynthesis and, accumulating in the tissues, inhibited vitamin

phosphorylation reactions.

PMID: 8619301 [PubMed - indexed for MEDLINE]

J Am Coll Nutr. 1994 Apr;13(2):144-8.

Glycolysis abnormalities in fibromyalgia.

Eisinger J, Plantamura A, Ayavou T.

Department of Rheumatic Diseases--Centre Hospitalier, Toulon, France.

OBJECTIVE: Primary fibromyalgia (FM) is a painful condition,

generally treated by analgesic drugs and antidepressants, which has

been associated with hyperpyruvicemia and reduced high energy

phosphate in muscle. Biological investigations were performed in

patients with FM to determine whether this syndrome was related to

carbohydrate metabolism impairment. METHOD: Glycolysis was studied in

25 patients with FM, 10 patients with hypothyroidism (HO), 15 patients

with osteoarticular chronic pain (OACP), and 36 healthy controls.

Laboratory studies were performed on whole blood (pyruvate),

erythrocytes (pyruvate kinase, 2-3 diphosphoglycerate, glyceraldehyde

phosphodeshydrogenase, adenosine triphosphate), plasma and serum

(lactate at rest and after forearm ischemic exercise, lactico

deshydrogenase iso-enzymes). RESULTS: Comparisons between study groups

and controls demonstrated increased pyruvate and decreased lactate

production in FM and HO; adenosine triphosphate and muscular

isoenzymes of lacticodeshydrogenase were decreased in FM only;

glycolysis was not significantly impaired in OACP. CONCLUSIONS: These

findings provide support that FM is associated with biochemical

abnormalities which require appropriate metabolic therapy.

PMID: 8006296 [PubMed - indexed for MEDLINE]

Here are some more articles by Eisinger that are probably worth a look:

J Am Coll Nutr. 1998 Jun;17(3):300-2.

Comment on:

* J Am Coll Nutr. 1998 Jun;17(3):300.

Alcohol, thiamin and fibromyalgia. (full text available at

http://www.jacn.org/)

Eisinger J.

Publication Types:

* Comment

* Letter

PMID: 10691388 [PubMed - indexed for MEDLINE]

J Am Coll Nutr. 1997 Feb;16(1):96-8.

Comment on:

* J Am Coll Nutr. 1996 Jun;15(3):197-8.

* J Am Coll Nutr. 1996 Jun;15(3):231-6.

Thiamin and cognitive impairment.

Eisinger J.

Publication Types:

* Comment

* Letter

PMID: 9013441 [PubMed - indexed for MEDLINE]

Rev Med Interne. 1994 May;15(6):387-9. Related Articles, Links

[Erythrocyte transketolases and Alzheimer disease]

[Article in French]

Eisinger J, Arroyo P, Braquet M, Arroyo H, Ayavou T.

Service de rhumatologie et medecine geriatrique, hopital

s-Clemenceau, Toulon, France.

Abnormalities of thiamin metabolism have been reported in senile

dementia of Alzheimer's type (SDAT). Transketolases (TK) were studied

in 21 patients with SDAT, 24 age-matched controls and 12 chronic

alcoholics. Erythrocytes were assessed for their TK activity

coefficient (TK-AC, normal value 8.4 +/- 12.6%) and affinity for

thaimin pyrophosphate (Km TPP, normal value 17.8 +/- 8.3 mumol).

Comparison between study groups and controls demonstrated increased

TK-AC in SDAT (16.6 +/- 15.7%, P < 0.05) and chronic alcoholism (43.4

+/- 40.6%, P < 0.05), and increased Km TPP (38.3 +/- 25.2 mumol, P <

0.01) in SDAT only. These findings suggest structural abnormalities of

TK rather than vitamin B1 deficiency in SDAT.

PMID: 8059170 [PubMed - indexed for MEDLINE]

Magnes Res. 1994 Mar;7(1):59-61. Related Articles, Links

Effects of magnesium, high energy phosphates, piracetam and

thiamin on erythrocyte transketolase.

Eisinger J, Bagneres D, Arroyo P, Plantamura A, Ayavou T.

Department of Rheumatology, C.H.I. Toulon, La Seyne/mer, France.

Erythrocyte transketolase activity coefficient (ETK-AC) and

affinity for coenzyme (Km TPP) were assessed in 50 patients with

transketolase abnormalities such as fibromyalgia or senile dementia of

Alzheimer's type, before and after magnesium (Mg), thiamin+pyridoxine

(B1,B6), high energy phosphates (HEP) (phosphocreatinine of adenosine

triphosphate), and piracetam. Compared to 12 untreated patients,

ETK-AC was significantly decreased with B1,B6 (P < 0.05, n = 10);

Km-TPP was significantly decreased with HEP (P < 0.05, n = 20) and

piracetam (P < 0.01, n = 5). In nine other patients treated with HEP +

B1,B6 + magnesium, ETK-AC and Km TPP were both significantly decreased.

PMID: 8054263 [PubMed - indexed for MEDLINE]

Postgrad Med J. 1998 Apr;74(870):229-32.

Comment in:

* Postgrad Med J. 1998 Nov;74(877):701.

Phosphate diabetes in patients with chronic fatigue syndrome.

De Lorenzo F, Hargreaves J, Kakkar VV.

Beatrice Research Centre, London, UK.

Phosphate depletion is associated with neuromuscular dysfunction

due to changes in mitochondrial respiration that result in a defect of

intracellular oxidative metabolism. Phosphate diabetes causes

phosphate depletion due to abnormal renal re-absorption of phosphate

be the proximal renal tubule. Most of the symptoms presented by

patients with phosphate diabetes such as myalgia, fatigue and mild

depression, are also common in patients with chronic fatigue syndrome,

but this differential diagnosis has not been considered. We

investigated the possible association between chronic fatigue syndrome

and phosphate diabetes in 87 patients who fulfilled the criteria for

chronic fatigue syndrome. Control subjects were 37 volunteers, who

explicitly denied fatigue and chronic illness on a screening

questionnaire. Re-absorption of phosphate by the proximal renal

tubule, phosphate clearance and renal threshold phosphate

concentration were the main outcome measures in both groups. Of the 87

patients with chronic fatigue syndrome, nine also fulfilled the

diagnostic criteria for phosphate diabetes. In conclusion, we report a

previously undefined relationship between chronic fatigue syndrome and

phosphate diabetes. Phosphate diabetes should be considered in

differential diagnosis with chronic fatigue syndrome; further studies

are needed to investigate the incidence of phosphate diabetes in

patients with chronic fatigue syndrome and the possible beneficial

effect of vitamin D and oral phosphate supplements.

PMID: 9683977 [PubMed - indexed for MEDLINE]

And here's another one that might be relevant for fibromyalgia:

Rev Rhum Engl Ed. 1995 Mar;62(3):175-81.

Adult-onset idiopathic phosphate diabetes. I. Chronic

pseudoinflammatory back pain and osteopenia.

Amor B, Clemente-Coelho PJ, Rajzbaum G, Poiraudeau S, Friedlander G.

Clinique de Rhumatologie, Hopital Cochin, Paris.

STUDY OBJECTIVE: to investigate clinical, laboratory test, and

bone mineral density abnormalities in 19 adults with phosphate

diabetes of unknown etiology diagnosed in a rheumatology department on

the basis of a maximal rate for tubular reabsorption of phosphate

(TmPO4/GFR) of 0.77 or less. RESULTS: there were 14 males and five

females with a mean age of 36.7 years (range 20 to 68 years) at

symptom onset and 43.9 years (24-70) at diagnosis. Seventeen patients

(90%) had back pain and 13 (68%) had nerve root pain. The pain was

nocturnal only or both nocturnal and diurnal in 14 cases (74%). Other

manifestations were fatigue (n = 7, 37%), myalgia (n = 6, 32%),

fracture (n = 6, 32%), renal colic (n = 4, 21%), and pseudodepression

(n = 10, 53%). Laboratory test abnormalities were as follows: serum

phosphate, 0.72 mmol/L (0.58-0.89); rate for tubular reabsorption of

phosphate, 74% (54-84%); maximal rate for tubular reabsorption of

phosphate, 0.58 (0.4-0.76); urinary calcium/urinary creatinine > 0.48

in nine patients (47%); and fractional potassium excretion > 20% in

seven patients (37%). Normal values were found for serum levels of

Ca++, Na++, Mg++, creatinine, cortisol, T3, T4, TSH, 25(OH)D3, and

1,25(OH)2 D3. Tests for glycosuria and amino aciduria were negative.

Bone mineral density measurements showed z-scores of -2.13 (+0.9 to

-4.25) at L2-L4, and -1.34 (+1.5 to -3.2) at the femoral neck. Bone

histology showed osteoporosis with a mild increase in osteoid

deposition. CONCLUSIONS: idiopathic adult-onset phosphate diabetes

manifests as chronic back pain and nerve root pain, sometimes with

fatigue and depression. Bone mineral density values are decreased and

histology shows osteopenia. Differential diagnoses include

spondyloarthropathy, disk disease, fibromyalgia, and depression.

Determination of the maximal rate for tubular reabsorption of

phosphate is the only means of establishing the diagnosis.

PMID: 7788334 [PubMed - indexed for MEDLINE]

J Am Coll Nutr. 1990 Feb;9(1):56-7.

Transketolase stimulation in fibromyalgia.

Eisinger J, Ayavou T.

Rheumatology Service, General Hospital, Toulon, France.

Publication Types:

* Clinical Trial

PMID: 2407767 [PubMed - indexed for MEDLINE]

Here is the link again to Kim Allsup's original newsgroup postings:

http://tinyurl.com/cyeo3

MarkM